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LAMP > GI Disease > Flashcards

GI Disease Flashcards

1
Q

How do you diagnose acute pancreatitis?

A

For diagnosis of acute pancreatitis, need 2 of 3:
– Abdominal pain characteristic of disease
– Amylase and/or lipase elevated at least 3x upper limit of normal (ULN)
– Characteristic imaging findings

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2
Q

Why is lipase (compared to amylase) often preferred in diagnosing pancreatitis?

A

• Lipase is preferred: more sensitive and
more specific for acute pancreatitis
• Neither enzyme has accepted prognostic value
• Lipase remains elevated longer than amylase
• Current recommendations are for lipase measurement alone.

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3
Q

How does sensitivity/specifity compare for diagnosis of pancreatitis w/ lipase and amylase?

A

Lipase: 90/93
Amylase: 78/92

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4
Q

What else besides acute pancreatitis can cause elevations in pancreatic enzymes?

A
  • Macroamylasemia/macrolipasemia
  • Renal failure
  • Acute appendicitis
  • Cholecystitis
  • Intestinal ischemia or obstruction
  • Peptic ulcer disease
  • Gynecological disease
  • Diabetes (higher lipase, so diagnostic cutoff is >3-5 ULN, but no consensus on actual value)
  • Parotid/salivary gland disease (amylase only)
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5
Q

What are causes of acute pancreatitis?

A
  • Gallstones and alcohol are most common
  • Hypercalcemia, hypertriglyceridemia
  • Post-ERCP, trauma/injury
  • Genetic pancreatitis(e.g.,CFmutations)
  • Drugs (e.g., azathioprine, sulfonamides, NSAIDs, steroid, tetracycline)
  • Viral infections (e.g., mumps, rubella, EBV, CMV, hepatitis)
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6
Q

bruising around umbiliccus

A

cullens

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7
Q

bruising around spleen/flank

A

greys

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8
Q

What are first tier LFTs?

A 
• Transaminases
– ALT, AST
• Bilirubin
• Alkaline phosphatase, γ-glutamyl transferase (GGT)
• Albumin
• Prothrombin time/INR
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9
Q

What are second tier LFTs?

A 
• Hepatitis viral serologies and molecular
tests
• Fe, ferritin, Cu
• Alpha-1 antitrypsin
• Autoantibody tests
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10
Q

What are the three classifiaitons of liver disease?

A
  1. hepatocellular injury/necrosis (damage/death to hepatocytes)
    ALT,AST > AP
  2. Cholestatic (obstruction of bile outflow from liver)
    AP > ALT or AST
  3. Infiltrative (neoplasm, amyloid)
    elevated AP w/ normal ALT, AST or AP > ALT, AST
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11
Q

What are transaminases and how do they differ?

A

• ALanine aminotransferase (ALT) (SGPT)
• ASpartate aminotransferase (AST) (SGOT)
• These “leak” from damaged hepatocytes
• ALT is more SPECIFIC for LIVER disease
– AST is found in MUSCLE and RED
– With extensive muscle breakdown, both ALT and AST rise
• ALT has a LONGER half-life

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12
Q

Where does AP come from?

A 
• Present on hepatocyte membrane
bordering the bile canaliculi
• Isoenzymes: liver, bone, placenta
– Elevation is not a specific marker for liver disease
• Bone, GI, kidney
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13
Q

When would you order GGT?

A

to confirm a liver source

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14
Q

What are reference intervals for AST/ALT?

A

• AST 0-45 U/L, female; 0-55 U/L, male
– Children higher to age 2
• ALT 0-50 U/L, female; 0-70 U/L, male

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15
Q

What are reference intervals for AP?

A

• Alkaline phosphatase 40-150 U/L

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16
Q

What are markers of liver function?

A

• Albumin
– Half-life of 21 days, but can fall more rapidly with severe inflammation
– Can fall with renal or GI losses, or burns
• Prothrombin time (PT, INR)

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17
Q

What causes an acute rise in transaminases?

A 
HepA/B
Drug induced hepatitis
Alcoholic
Ischemic (shock liver)
Acute duct obstruction
Wilson disease
Autoimmune hepatitis
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18
Q

Diagnostic test: Hep A

A

IgM anti-HAV

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19
Q

Diagnostic test: Hep B

A

HBsAg, IgM angti-HBc

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20
Q

Diagnostic test: drug induced hepatitis

A

improvement on stopping

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21
Q

Diagnostic test: alcoholic

A

liver bx
improvement iwth abstinence
AST:ALT >2
AST <400

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22
Q

Diagnostic test: shock liver

A

improvement iwth restoration of circulation

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23
Q

Diagnostic test: acute duct obstruction

A

cholangiography

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24
Q

Diagnostic test: wilson disease

A

ceruloplasmin
urine copper
slit lamp
liver Cu measurement

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25
Q

Diagnostic test: autoimmune hepatitis

A

anti-smooth muscle (f actin)

anti-LKM type 1

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26
Q

How high can ALTL be with acute hepatitis?

A

thousands

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27
Q

If ALT over 5000 consider….

A

acetaminophen
hepatic ischemia
unusual viruses like HSV

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28
Q

stones can cause transient elevations to…

A

1000s

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29
Q

alcoholic hepatitis cuases modest elevations to…

A

less than 400 (bili is often elevated more)

30
Q

What are common cuases of chronic hepatitis?

A

HepC/B (anti-HCV, RNA, HBsAg)
NASH (US, liver bx)
Alscoholic liver disease (liver bx)

31
Q

How do you define chronic hepatitis?

A

> 3 mos
transaminases usually 205 fold elevated
pt can be asymptomatic

32
Q

what characterizes cholestatic disrorders?

A

rise in AP and bili

33
Q

blockage of microscopic ducts

A

primary biliary cholangitis

34
Q

blockage of large ducts

A

obstruction
ca of head of pancreeas
stones

35
Q

blockage of large and small dcuts

A

primary sclerosing cholangitis

36
Q

What are common causes of cholestasis?

A 
PBC
PSC
Large bile duct obstruction
drug induced
infiltrative/malignancy
inflammation
37
Q

Middle-aged women

Anti-mitochondrial antibody

A

Primary biliary cholangitis

38
Q

Usually men 20-50; ulcerative colitis

Cholangiography

A

primary sclerosing cholangitis

39
Q

Jaundice, pain

Ultrasound

A

large bile duct obstruction (stone, tumor)

40
Q

Malignancy, sarcoid, amyloid

Ultrasound, CT

A

drug induced

41
Q

adult bili ref range

A

.2 - 1.3

42
Q

first 2 wks of life bili

A

0-11.7

43
Q

bilirubinuria is = …

A

lier disease

44
Q

> 85%
insoluble, carried by albumin
elevation means hemolysis

A

unconjugated/indirect

45
Q

<15%
soluble
elevations mean liver disease (parenchyma/biliary tract)

A

conjugated/direct

46
Q

When is jaundice visible?

A

bili > 2.5 mg/dL

47
Q

What causes unconjugated hyperbilirubinemia?

A

• Hemolysis, resorption of a large hematoma,
ineffective erythropoiesis (e.g., B12 deficiency)
• Neonatal physiologic hyperbilirubinemia
• Gilbert syndrome

48
Q

What is Gilbert syndrome?

A 
– Benign defect in UDPGT activity
– 3-7% of the population, M:F 2-7:1
– Manifests in stress conditions, including fasting – Bilirubin < 6.0 mg/dL
– LFTs normal, Hb normal
– No treatment, just reassurance
49
Q

What suggests conjugated hyperbijjlirubinemia?

A

– Suggested by abdominal pain, fever, palpable gall bladder
– Ultrasound reveals duct dilation, unless very transient (e.g., passage of a gall stone)
– A transient rise in aminotransferase levels can be seen with acute large duct obstruction

50
Q

alcoholic hepatitis

A
  • Hepatocellular injury
  • AST> 2xALT, but AST <400UL
  • Bilirubin increase and PT/INR better indices
51
Q

What viruses classically cuase viral hepatitis?

A

Hep A, B (D,C,E)
CMV
EBV
HSV

52
Q

What should you exclude before diagnosing autoimmune hepatitis?

A

chronic viral hepatitis
wilson disease

assoc w/ Hashimotos thyroiditis

53
Q

WHat is primary biliary cirrhosis?

A
  • Typically middle aged women (40-60 yrs)
  • Presents with fatigue and pruritus
  • Increased levels of AP and IgM
  • Fat soluble vitamin deficiencies and metabolic bone disease, increased cholesterol (HDL), later increased bilirubin
  • Granulomatous infiltration of septal bile ducts
  • Anti-mitochondrial antibodies present in over 90-95%
54
Q

Autoimmune hepatitis vs PBC

A

Autoimmune hepatitis:
7-10x ULN
anti-smooth muscle Ab 90%

PBC:
1-3xULN
anti-mito 90-100%

55
Q

What causes toxic hepatitis?

A 
• Alcohol
• Drugs
– Predictable (e.g., acetaminophen) – Idiosyncratic (e.g., isoniazid)
• Environmental
– Vinyl chloride
– Jamaica bush tea
– Kava kava
– Amanita phalloides or A. verna (mushrooms)
56
Q

acetaminophen toxicity: 0-24 hrs

A

Anorexia, nausea, vomiting

57
Q

acetaminophen toxicity: 24-72

A

Right upper quadrant abdominal pain (common)

AST, ALT, and, if poisoning is severe, bilirubin and PT (usually reported as the INR) sometimes elevated

58
Q

acetaminophen toxicity: 72-96

A

Vomiting and symptoms of liver failure Peaking of AST, ALT, bilirubin, and INR Sometimes renal failure and pancreatitis

59
Q

acetaminophen toxicity: >5

A

Resolution of hepatotoxicity or progression to multiple organ failure (sometimes fatal)

60
Q

What is hte rumack matthew nomogram

A

Hours vs. Plasma acetaminophen (can determine if hepatotoxicity likely given level and how many hours out)

61
Q

What causes Fe overload?

A

Herediatary hemochromatosis
Multiple blood transfusions (talassemia major)
Consider in adults w/ liver disease (men)

62
Q

What should you consider in a pt with transferrin saturation >55% and ferritin > 200?

A

Fe overload

Liver bx with Fe measurement

63
Q

Where does Cu accumulate in wilsons disease?

A

liver

basal ganglia

64
Q

defect in wilson disease

A

ATP7B gene (increased Cu absorption, decreased excretion)

65
Q

What are sxs of Wilson diesase?

A
  • Hepatitis, splenomegaly, hypersplenism, Coombs neg. hemolytic anemia, portal hypertension, neuro-psychiatric disease
  • Can cause chronic or fulminant hepatitis
  • Kayser-Fleischer ring seen on slit-lamp exam
66
Q

Wilson disease is usually diagnosed in what population?

A

adolescent or young adult

67
Q

Labs diagnostic of WIlsons?

A
  • Increased urinary Cu (> 40 μg/24 h)
  • Low serum ceruloplasmin (<20 mg/dL; <5 mg/dL is diagnostic) (Cu binding protein)
  • Increased hepatic Cu (>250 μg/g dry wt.)
68
Q

What is Crigler Najjar type 1?

A
  • Very rare, newborns
  • Unconjugated hyperbilirubinemia
  • Bilirubin > 20 mg/dL
  • Fatal disease, kernicterus – Liver transplant
  • ABSENT UDPGT activity
69
Q

What is Crigler Najjar type 2?

A 
• More common than type 1
• Unconjugated hyperbilirubinemia • Can survive to adulthood
• Bilirubin 5-25 mg/dL
• Milder DEFICIENCY of UDPGT
– Enzyme can be induced by phenobarbital
70
Q

What are dubin johnson and rotor syndromes?

A
  • Both are rare, benign disorders with asymptomatic jaundice
  • Often present in 2nd decade of life
  • Increased direct (conjugated bilirubin)
  • Dubin-Johnson caused by mutations in multiple drug resistance protein 2
  • Rotor syndrome mechanism unclear
71
Q

Neonatal jaundice affects what % of newborns?

A

60%

acute encephalopathy > kernicterus

72
Q

What causes neonatal jaundice

A

• Usually immaturity of conjugating enzymes
• Other causes
– Hemolytic disease (incl. HDN), bruising (e.g.,
cephalohematoma)
– Breast feeding, especially if inadequate – Sepsis

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